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NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION
Circulatory Control Laboratory, Department of Physiology and Bioengineering Institute, University of Auckland, Auckland, New Zealand
Submitted 11 July 2005 ; accepted in final form 17 October 2005
We have explored the possibility that renal sympathetic nerve activity (RSNA) and vasomotor sympathetic nerve activity are differentially regulated. We measured sympathetic nerve activity (SNA) to the kidney and the hind limb vasculature in seven conscious rabbits 68 days after the implantation of recording electrodes. Acute infusion of NG-nitro-L-arginine methyl ester (L-NAME) (6 mg·kg1·min1 for 5 min) led to an increase in blood pressure (from 66 ± 1 to 82 ± 3 mmHg) and a decrease in heart rate (from 214 ± 15 to 160 ± 13 bpm). L-NAME administration caused a significantly greater decrease in RSNA than lumbar sympathetic nerve activity (LSNA) (to 68 ± 14% vs. 84 ± 4% of control values, respectively). Volume expansion (1.5 ml·kg1·min1) resulted in a significant decrease in RSNA to 66 ± 7% of control levels but no change in LSNA (127 ± 20%). There was no difference in the gain of the baroreflex curves between the LSNA and RSNA [maximum gain of 7.6 ± 0.4 normalized units (nu)/mmHg for LSNA vs. 7.9 ± 0.75 nu/mmHg for RSNA]. A hypoxic stimulus (10% O2 and 3% CO2) led to identical increases in both RSNA and LSNA (195 ± 40% and 158 ± 21% of control values, respectively). Our results indicate tailored differential control of RSNA and LSNA in response to acute stimuli.
sympathetic activity; blood pressure
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